Authors

Date of this Version

1992

Citation

HORTSCIENCE 27(4):373. 1992

Comments

Copyright 1992 American Society for Horticultural Science. Used by permission.

Abstract

Scorch of rhizomatous iris, Iris spp., occurs throughout much of the United States (Black, 1984). It is characterized as a rustcolored browning that starts on the tips of the youngest leaves in the center of the fan. Leaf necrosis progresses downward on the leaves and outward on the fan until the entire fan is affected. Roots shrivel and decay. Root cortical tissue completely deteriorates, but the epidermis and stele remain intact. The rhizome appears unaffected (Wadekamper, 1972).

Because of the sporadic occurrence of scorch and the difficulty of artificially reproducing scorch symptoms, little is known about the etiology, epidemiology, or the pathogenicity of organism(s) involved in its development (Black, 1984). Attempts to identify a predominant causal organism or transmit scorch through inoculation with various fungi and bacteria recovered from scorched iris have failed to reproduce the disease (Wadekamper, 1972).

Bald (1971) implicated the bacterium Pseudomonas gladioli pv. gladioli (Severini) as the probable cause of iris scorch. He obtained evidence of pathogenicity by inoculating wounded iris tissue with cell suspensions of the Pseudomonas bacterium. However, symptoms were less severe than those that occurred in the field under natural disease development. Rainio (1936) reported that P. marginata, synonymous with P. g. pv. gladioli, entered the iris leaf through wounds, where it caused a localized watersoaked wet rot but not the characteristic scorch symptoms.

Since the pathogenicity of P. g. pv. gladioli to rhizomatous iris is not clear, the present study was undertaken to determine if P. g. pv. gladioli could be recovered from scorched iris and to characterize the symptoms produced by inoculation of rhizomatous iris with P. g. pv. gladioli.